Shock

Shock is a life-threatening circulatory disorder that leads to tissue hypoxia and a disturbance in microcirculation. The numerous causes of shock are classified into hypovolemic shock (e.g., following massive blood/fluid loss), cardiogenic shock (e.g., as a result of acute heart failure), obstructive shock (e.g., due to cardiac tamponade), and distributive shock (due to redistribution of body fluids), which is further classified into septic, anaphylactic, and neurogenic shock. Common clinical findings are hypotension and abnormal heart frequency (most commonly tachycardia; bradycardia in neurogenic shock) accompanied by specific symptoms related to the cause of shock. Diagnosis is mostly clinical but measurement of functional parameters (e.g., PCWP, cardiac output, SVR) can help distinguish between the different types of shock. Management of shock involves circulatory support and treatment of the underlying cause. Shock is associated with a very high mortality rate.

Definitions

• Shock (circulatory shock): a life-threatening disorder of the circulatory system that results in inadequate organ perfusion and tissue hypoxia, leading to metabolic disturbances and, ultimately, irreversible organ damage ^[1][2]
• Shock index = pulse rate/systolic blood pressure
  • Normal range: 0.4–0.7
  • > 1 (positive shock index): consistent with circulatory shock

Types of shock

Hemodynamic parameters in shock

Stages of shock

The following stages may not occur in cases of sudden severe cardiovascular collapse , and the progression between stages in septic shock can be indistinct.

• Patients may present at the emergency department with shock or develop shock at any time during hospitalization.
• Screening for clinical features of shock in patients at risk can allow for early identification and treatment.
• The clinical picture may vary depending on the stage of shock.

Hypotension may be absent in some patients with shock. ^[7]

Signs of congestive heart failure alongside shock (e.g., ↑ JVP, crackles on lung auscultation) are suggestive of cardiogenic shock.

Approach ^[4][7][8]

The following should be performed simultaneously:

• Perform ABCDE survey: Identify the need for immediate airway or breathing intervention (e.g., basic airway maneuvers, supplemental O₂).
• Establish vascular access immediately: Simultaneously obtain blood samples for testing.
  • Preferred: ≥ 2 large-bore proximal peripheral IVs
  • Alternatives
    • IO access
    • Central venous line (CVL)
• Begin immediate hemodynamic monitoring.
  • Continuous cardiac monitoring and pulse oximetry
  • Consider invasive monitoring for severe shock (e.g., central venous pressure, arterial line).
• Classify the type of shock (see “Overview of types of shock”).
  • Check vital signs, signs of end-organ hypoperfusion, and other distinguishing clinical features.
  • Identify likely etiology of shock.
  • Perform rapid diagnostic studies, e.g., POCUS, portable CXR, ECG, serum lactate, ABG/VBG.
• Provide immediate hemodynamic support: can be started for undifferentiated shock
  • Begin fluid resuscitation immediately if there are no clinical signs of fluid overload or diagnostic evidence of cardiogenic shock.
  • Consider a fluid challenge or passive leg raise test if fluid responsiveness is in doubt.
  • Determine the need for vasopressors, inotropes, or blood transfusions.
  • Determine the need for other critical therapy (e.g., corticosteroids for adrenal crisis, epinephrine for anaphylaxis, needle thoracostomy for tension pneumothorax).
• Call for help early: critical care consult or rapid-response team
• Frequently reassess the patient (e.g., for signs of deterioration or response to therapy): Consider advanced hemodynamic monitoring parameters.
• Start specific management: according to the identified mechanism and its cause
  • Hypovolemic shock
  • Cardiogenic shock
  • Obstructive shock
  • Distributive shock

Act quickly: Provide immediate hemodynamic support and simultaneously try to identify the type of shock and the underlying cause in order to provide appropriate treatment.

Patients in shock are at risk of cardiopulmonary arrest; if the pulse is lost, start CPR!

Management of patients with severe shock can be recalled with the VIP rule: Ventilation as needed, Infuse IV fluids, and Pump vasopressors as needed. ^[4]

Routine investigations can help identify the shock subtype but are not required for diagnosis. Consider further investigations if the subtype remains uncertain.

Shock is a clinical diagnosis.

Routine investigations

Findings allow for evaluation of the following:

• Global hypoperfusion
  • ↑ Lactate (> 2 mEq/L) suggests tissue hypoperfusion
  • ABG
    • Metabolic acidosis: ↑ base excess, ↓ HCO₃^-
    • Contraction alkalosis: ↑ HCO₃^-
• Underlying etiology
  • CBC
    • ↓ Hb, ↓ Hct: suggests hemorrhage
    • Leukopenia or leukocytosis: suggests sepsis
  • BMP: ↑ BUN/Cr ratio, hyponatremia, and other laboratory findings of hypovolemia
  • Septic workup: e.g., urinalysis, blood cultures
  • ECG: Findings can show evidence of cardiogenic etiology, e.g., arrhythmias , acute coronary syndrome , signs of cardiomyopathy.
  • CXR
    • Pneumonia : suggests sepsis
    • Pulmonary edema , cardiac enlargement, or pleural effusions : suggests cardiogenic etiology
    • Pneumothorax : suggests obstructive etiology
• Complications or end-organ dysfunction
  • Hypoglycemia or hyperglycemia
  • Electrolyte abnormalities
  • Renal function tests: ↑ BUN, ↑ creatinine, other signs of AKI or ATN (e.g., on urinalysis)
  • Liver chemistries: elevated in shock liver
  • Coagulation panel: suggestive of DIC, acute traumatic coagulopathy, or acute liver failure

In all patients with shock, immediately measure ABGs, lactate levels, capillary glucose, perform an ECG, and order a chest x-ray and general laboratory studies.

Compare any available previous studies to the patient's current test results. Previous studies can help determine if alterations to any laboratory or imaging studies are new and likely the cause of shock, or if they are caused by chronic conditions (e.g., CKD, chronic heart failure).

Further investigations

Further studies should be guided by clinical suspicion of the underlying cause.

If hemorrhagic shock is suspected, perform blood type and screen and crossmatch immediately. In emergencies, O-negative blood can be given immediately; however, type-specific and crossmatched blood products are preferred as soon as they are available.

Bedside echocardiography

Simplified cardiac ultrasound can help identify pericardial effusion and indirect signs of right heart failure and cardiomyopathy. ^[12][13]

IVC ultrasound ^[14][15][16]

Changes in IVC collapsibility can help predict fluid responsiveness, e.g., after a fluid challenge or passive leg raise test. ^[17]

Additional point-of-care ultrasound ^{[16][21][22][23]}

• eFAST: can help identify intraperitoneal free fluid and pneumothorax
• Limited abdominal ultrasound: can help identify AAA
• Lung ultrasound findings: Parameters measured include pulmonary A-lines and B-lines and the seashore sign. ^[14][23]
  • Pleural effusion: hypoechoic pleural fluid accumulations (> 5–20 mL)
  • Pneumothorax: absent lung sliding (e.g., on M-mode) or unilateral loss of B-lines
  • Pulmonary fluid overload: bilateral diffuse B-lines (> 3 B-lines visible within an intercostal space are suggestive of interstitial edema)
  • Consolidations in pneumonia: hyperechoic and irregular lung tissue ^[23]

Monitoring parameters can be used as treatment targets and should be tailored to the patient.

Signs of an inadequate response to fluid resuscitation include persistently ↑ heart rate, ↓ blood pressure, ↓ CVP, and ↓ urine output (< 0.5 mL/kg/hour).

• Invasive monitoring procedures: typically reserved for patients with severe shock
  • Most patients: urinary catheter to assess urine output
  • Patients requiring vasopressors ^[7]
    • Central venous line: can be used for CVP monitoring and ScVO₂ sampling
    • Arterial line: can be used for invasive blood pressure monitoring and frequent ABG sampling
  • Select patients with refractory shock, RV dysfunction, or high risk of pulmonary edema with uncertain fluid status: pulmonary artery catheterization ^[7][31]
• Protocolized resuscitation targets: e.g., consider lactate-guided fluid resuscitation strategy or early goal-directed therapy (EGDT) in sepsis.

IV fluid resuscitation

Start with glucose-free isotonic crystalloids. ^[32]

• Clearly apparent _Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">hypovolemia
  • IV fluid bolus over 20–30 minutes ^[4][7]
    • Adults: NS or lactated Ringer's 500–1000 mL IV bolus
    • Children: NS or lactated Ringer's 20 mg/kg IV bolus
  • Hemorrhagic shock: Transfuse blood products as needed; replace blood losses with blood.
• Uncertain _Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">hypovolemia (of particular concern in patients at risk for fluid overload) ^[7][24][33]
  • Assess fluid responsiveness: e.g., perform a fluid challenge or a passive leg raise and guide therapy accordingly. ^[33]
    • No response to IV fluids: Stop IV fluid boluses; start vasopressors or inotropes. ^[33]
    • Fluid responsive: Repeat fluid challenge until there is no longer a response.
• Next steps (patient has been stabilized)
  • Continue with volume titration; further fluid challenges can be performed.
  • Proceed with other strategies for IV fluid therapy according to the patient's needs.

Vasopressors ^[4]

• Indications: treatment of various shock states in an effort to restore adequate arterial pressure and organ perfusion
  • Start immediately if hypotension is severe (simultaneously perform volume resuscitation).
  • Start in patients who are not fluid responsive following adequate IV fluid resuscitation.
• Available agents
  • Choice is determined based on the underlying shock physiology, the desired pharmacological effects, and potential adverse effects.
  • First-line in undifferentiated shock: norepinephrine
• Next steps
  • Adjust infusion according to hemodynamic monitoring parameters.
  • Titrate down as soon as possible until the patient is weaned.

Patients with chronic corticosteroid use need steroid stress dosing to prevent adrenal crisis!

General principles ^[3][35]

• Vasopressors
  • Most vasopressors are inoconstrictor drugs.
    • Vasoconstriction → ↑ SVR → ↑ BP
    • Inotropy → ↑ cardiac contractility → ↑ CO and ↑ MvO₂
  • Some are pure vasoconstrictor drugs: ↑ SVR without either significant ↑ cardiac contractility or ↑ HR
  • All have varying degrees of dose-dependent chronotropic effects.
  • Increasingly high dosages can be harmful because of:
    • Risk of ↓ peripheral tissue perfusion > benefits of ↑ systemic BP
    • ↑ Tachycardia → ↓ diastolic filling time → ↓ stroke volume → ↓ CO
    • ↑ SVR → ↑ afterload → ↑ MvO₂ → ↑ cardiac dysfunction (especially if there is underlying cardiomyopathy or coronary artery disease)
• Inodilators: unique mechanism of action
  • ↑ Cardiac contractility → ↑ CO
  • Peripheral vasodilation → ↓ SVR → ↓ afterload (combined with ↑ CO) → improved peripheral blood flow and tissue perfusion

Blood pressure does not always correlate with blood flow. Agents that increase blood pressure through vasoconstriction can impair tissue perfusion at high doses.

Although certain vasopressors, inotropes, and inodilators can be combined (e.g., to allow for individual agents to be used in moderate doses), this requires careful titration and specialist consultation.

Etiology

• Hemorrhage
  • Postpartum hemorrhage
  • Upper GI bleeding (e.g., variceal bleeding, PUD)
  • Blunt/penetrating trauma
  • Ruptured aneurysm or hematoma
  • Arteriovenous fistula
• Nonhemorrhagic fluid loss
  • GI loss (e.g., diarrhea, vomiting)
  • Increased insensible fluid loss (e.g., burns)
  • Third space fluid loss (e.g., bowel obstruction, pancreatitis)
  • Renal fluid loss (e.g., adrenal insufficiency, drug-induced diuresis)

Pathophysiology

Loss of intravascular fluid volume → ↓ preload and SV → ↓ CO → compensatory ↑ SVR and HR

Management ^[4][7][8]

The priority of immediate hemodynamic support is aggressive fluid resuscitation to achieve euvolemia. Further treatment depends on the etiologic category of _Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">hypovolemia (hemorrhagic vs. nonhemorrhagic).

Hemorrhagic shock

• Blood products: Transfuse as soon as possible.
  • Ensure adequate vascular access and equipment (e.g., tubing) for blood products.
  • Consider emergency transfusion of uncrossmatched blood type O rhesus negative units.
  • Switch to crossmatched blood transfusions as soon as available.
  • If massive transfusion is expected : Consider transfusing packed RBC, FFP, and platelet concentrate in a 1:1:1 ratio. ^[47]
  • Consider the use of specialized infusers that allow for rapid administration of warmed blood.
• Hemostatic control: should be prioritized
  • Begin immediate bedside measures: e.g., applying pressure, suturing, or stapling open wounds.
  • Consult specialist based on underlying etiology and risk stratification: e.g., surgery, gastroenterology, OB-GYN, interventional radiology.
  • Ensure definitive care: See “Management of trauma patients,” ”Treatment of GI bleeding,” “Abnormal uterine bleeding,” “Antepartum hemorrhage,” and “Postpartum hemorrhage.”
• Additional steps to consider
  • Tranexamic acid for severe traumatic injury within 3 hours of injury ^[48][49]
  • Classification of hemorrhagic shock to help prioritize definitive care and monitor response to treatment

Upon suspecting hemorrhagic shock, perform blood grouping and cross-matching and have packed RBCs at hand for transfusion.

Uncrossmatched RBC type O negative units can be transfused if the hemorrhage is severe.

Nonhemorrhagic hypovolemic shock

• Treatment of the underlying etiology to stop fluid losses, including:
  • GI losses: e.g., antiemetics for nausea and vomiting, antidiarrheal drugs
  • Third space fluid loss: e.g., treatment for pancreatitis or bowel obstruction
  • Increased insensible fluid losses: e.g., treatment for burns, antipyretic therapy for fever
  • Renal losses: e.g., cessation of diuretics, treatment for diabetes insipidus
• Supportive care: e.g., treating any concomitant electrolyte abnormalities (e.g., hyponatremia, hypokalemia)
• Next steps (once hemodynamically stable)
  • Continue with replacement of ongoing fluid loss as needed.
  • Attempt oral rehydration therapy.

Etiology

• Myocardial infarction (MI): most common cause
• Arrhythmias
• Heart failure
• Cardiomyopathy
• Myocarditis
• Ventricular septal defect, ventricular rupture
• Valve defects: severe aortic or mitral regurgitation
• Blunt cardiac trauma
• Certain drugs (e.g., beta blockers, calcium channel blockers)

Pathophysiology

• Underlying event causes dysfunction of the heart → ↓ cardiac contractility and/or SV → ↓ CO
• Systemic circulation: ↓ CO and ↓ BP → ↑ catecholamines → vasoconstriction and ↑ myocardial oxygen demand → ↑ renin-angiotensin-aldosterone system → further ↑ vasoconstriction and retention of sodium and water → shunting of blood to the brain and vital organs → insufficient perfusion of peripheral organs
• Pulmonary circulation: ↓ cardiac contractility and/or ↓ SV → ↑ pulmonary hydrostatic pressure → pulmonary edema

Management approach ^[50]

• Determine the type of cardiogenic shock according to the classification of acute heart failure.
  • No evidence of congestion (“dry and cold”)
  • Evidence of congestion (“wet and cold”)
• Tailor initial treatment according to type.
• Provide supportive care.
  • Elevate the patient's head.
  • Provide respiratory support for AHF if there are signs of fluid overload.
  • Stop or modify medication that can worsen the symptoms (e.g., antihypertensives).
• Treat the underlying cause (e.g., revascularization in MI).
• See also “Management of acute heart failure.”

IV fluids can worsen cardiogenic pulmonary edema in most cases of cardiogenic shock. Check fluid responsiveness prior to administration of fluid therapy.

Avoid inotropes in patients with left ventricular outflow tract obstruction (e.g., hypertrophic cardiomyopathy, aortic stenosis). ^[54]

Etiology

• ↓ Diastolic filling
  • Cardiac tamponade
  • Constrictive pericarditis
  • Restrictive cardiomyopathy
• ↓ Venous return
  • Tension pneumothorax
  • Intrathoracic tumor
• ↑ Ventricular afterload
  • Massive pulmonary embolism (PE)
  • Aortic dissection
  • Aortic stenosis
  • Large systemic emboli
  • Severe pulmonary hypertension

Pathophysiology ^[6]

• Common mechanism: obstruction of the heart or its great vessels → inability of the heart to circulate blood → ↓ CO → compensatory ↑ SVR
• Pulmonary embolism or severe PAH
  • Obstructions of the pulmonary vasculature → ↑ PCWP → ↑ RV pressure → right heart failure
  • ↑ RV pressure → ↑ pressure on LV by the RV → ↓ LV diastolic filling → ↓ CO
  • Right heart failure → LV preload → ↓ CO
• Tension pneumothorax
  • ↑ Intrathoracic pressure → ↓ venous return → ↓ preload → ↓ PCWP
  • ↑ Intrathoracic pressure → ↓ LV diastolic filling → ↓ CO
• Cardiac tamponade
  • ↑ Pericardial pressure → ↑ RV pressure → ↓ RV diastolic filling → right heart failure
  • ↑ Pericardial pressure → ↑ LV pressure → ↓ LV diastolic filling → ↓ CO
  • ↑ LV pressure → ↑ PCWP → ↑ RV pressure
  • Right heart failure → ↓ LV preload → ↓ CO

Despite manifesting with high PCWP, many causes of obstructive shock (e.g., severe pulmonary hypertension, cardiac tamponade) are considered preload-dependent states. ^[6]

Elevation and equalization of pressures in all the cardiac chambers differentiate cardiac tamponade from other causes of obstructive shock.

Treatment

• Provide immediate hemodynamic support.
  • Fluid resuscitation for patients who are preload-dependent and/or fluid responsive
  • Consider vasopressors or inotropic support.
• Treatment based on the underlying cause, including:
  • Pericardiocentesis for cardiac tamponade
  • Thrombolytic therapy in PE or embolectomy in PE
  • Needle thoracostomy followed by chest tube placement or surgery for tension pneumothorax

Etiology

• Septic shock
  • Infection (especially gram-negative bacteria) and bacteremia
  • See “Etiology” in “Sepsis.”
• Anaphylactic shock
  • Drug reactions; (e.g., sulfa drugs, contrast medium allergy)
  • Insect stings or bites (e.g., bee stings)
  • Food allergies (e.g., peanuts)
• Neurogenic shock
  • Spinal cord injury (SCI)
  • Traumatic brain injury
  • Cerebral hemorrhage
  • Neuraxial anesthesia
• Acute adrenal insufficiency
  • Stress in patients with underlying adrenal insufficiency
  • Sudden discontinuation of glucocorticoids after prolonged glucocorticoid therapy
  • See “Adrenal crisis” for details.

Pathophysiology

• Common mechanism: vasodilation with or without capillary leakage → redistribution of fluid from the intravascular to the extravascular compartment
• Septic shock
  • Specific mechanisms
    • Dysregulated host response to infection → capillary leakage and systemic vasodilation → acute organ dysfunction
    • Circulating inflammatory cytokines → myocardial depression
  • Effect on cardiac output
    • Early: compensatory ↑ HR and contractility → ↑ CO (hyperdynamic state or “warm shock”)
    • Late: ↓ preload and direct myocardial depression by cytokines → ↓ CO (hypodynamic state or “cold shock”) ^[55]
• Neurogenic shock
  • Specific mechanism: damage of autonomic pathways → loss of sympathetic vascular tone → unopposed vagal tone → peripheral vasodilation → pooling of peripheral blood
  • Effect on cardiac output: can last days to weeks after spinal cord injury ^[56][57]
    • Unopposed vagal effect → ↓ HR
    • ↓ Catecholamines released from the sympathetic outflow → absent compensatory increases in HR and cardiac contractility
• Anaphylactic shock
  • Specific mechanism: immunologic anaphylaxis (type I hypersensitivity reaction; IgE-mediated) or nonimmunologic anaphylaxis (not IgE-mediated) → degranulation of mast cells → massive histamine release → systemic vasodilation and increased capillary leakage
  • Effect on cardiac output
    • Early: compensatory ↑ HR and ↑ SV → ↑ CO
    • Late: ↓ vascular tone and ↑ capillary permeability → ↓ venous return → ↓ CO → ↓ coronary perfusion → ↓ contractility → ↓↓ CO ^[58]

Key treatment components

• Volume expansion with fluid resuscitation
• Reversal of vasodilation with vasopressors
• Treatment of the underlying condition (e.g., antibiotics, removal of inciting allergens, spinal decompression surgery, glucocorticoid replacement)

Definition

• Sepsis and both of the following, despite adequate fluid therapy (i.e., normovolemic patients):
  • Vasopressors required to maintain an MAP ≥ 65 mm Hg
  • Serum lactate > 2 mEq/L (> 18 mg/dL)
• See also “Sepsis definitions” for details on qSOFA and SIRS criteria.

Management of septic shock

See “Management of sepsis” for details on evaluation and definitive treatment of sepsis. The following recommendations relate to septic shock and are consistent with the 2016 and 2018 Surviving Sepsis Campaign guidelines: ^[59][60]

• Begin interventions of the hour-1 bundle for sepsis, including:
  • Fluid resuscitation: rapid crystalloid infusion of 30 mL/kg ^[59][60]
  • Antibiotic therapy for sepsis
• Consider protocolized resuscitation target strategies in addition to standard hemodynamic monitoring parameters.
• The threshold for beginning vasopressors for septic shock should be low.
• Consider corticosteroids (e.g., hydrocortisone ) for shock refractory to the first vasopressor.

6–10 L of IV fluids may be necessary during the first 24 hours. ^[61]

Protocolized resuscitation target strategies ^[59][60][62]

• Lactate-guided fluid resuscitation strategy ^[60][62]
  • If the initial lactate level is elevated (> 2 mmol/L), remeasure every 2–4 hours until normalized.
  • Treatment target: 20% decrease in serum lactate every 2–4 hours until normal
    • Down-trending lactate: Continue fluid resuscitation until normalized.
    • Persistent hypotension and/or lactate does not decrease as expected: aggressive fluid resuscitation and consider adding vasopressors.
  • Disadvantages ^[62][63]
    • Elevated lactate is not specific to sepsis.
    • This strategy may lead to fluid overload.
• Early goal-directed therapy (EGDT) ^[59]
  • Treatment targets
    • CVP ≥ 8 cm H₂O ^[59]
    • Central venous O₂ saturation ≥ 70%
• MAP treatment target: ≥ 65 mm Hg

Vasopressors for septic shock ^{[59][60][62][63][64]}

• Indications: : persistent hypotension during or after fluid resuscitation
• Goal: maintain MAP ≥ 65 mm Hg ^[59]
• Stepwise escalation (see “Vasopressors and inotropes” for dosages)
  • First-line: norepinephrine
  • If MAP is still low after norepinephrine:
    • Add vasopressin
    • OR add continuous IV epinephrine infusion (off-label)
  • To decrease norepinephrine dosage: Add vasopressin.
• Additional options
  • Dopamine
    • Indicated as an alternative vasopressor in select cases (e.g., low risk of tachyarrhythmia, bradycardia) ^[59]
    • Should not be used for renal protection ^[59]
  • Dobutamine: Consider for hypoperfusion that persists despite fluids and initial vasopressors. ^[59]

Initial management ^[61][65][66]

• Assess and secure the airway as needed (see “Airway management and ventilation in anaphylaxis”).
• Remove allergen when possible (e.g., stop medication or IV contrast).
• Administer epinephrine IM 1:1,000 as soon as possible and repeat as needed.
• Provide immediate hemodynamic support with fluid resuscitation.
• See also “Management of anaphylaxis” for further details.

Adjunctive treatment (antihistamines and corticosteroids) should only be administered after the initial resuscitation measures (IM epinephrine, fluids and/or vasopressors) have been given.

Refractory anaphylactic shock ^[61][65][66]

• Refractory to repeated IM epinephrine and fluids: Start continuous IV epinephrine infusion 1:1,000,000 (1 mcg/mL).
• Refractory to IV epinephrine infusion
  • Administer IV glucagon , especially if the patient is on a beta blocker.
  • Consider combination with other vasopressors: e.g., vasopressin, norepinephrine, dopamine, and phenylephrine.
  • Ensure adequate fluid status.
  • Consider consulting ECMO team if all other measures fail.

Diagnosis

Neurogenic shock is a clinical diagnosis.

• Classic presentation: hypotension; , bradycardia, vasodilation ^[5]
• Exclude other reasons for shock (e.g., other injuries).
• Other neurological deficits may be present.

In a patient who develops low blood pressure following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after _Definitions"#Z2c4b7b192fbfa8d2679ddc134ed0e9c5" data-lxid="Ig0Y92">hypovolemic and obstructive shock have been ruled out.

Management ^[67][68][69]

• Treatment
  • Fluid resuscitation
    • First-line therapy
    • Avoid aggressive fluid boluses in patients with poor fluid responsiveness, because of the risk of fluid overload.
  • Vasopressors: commonly required as shock is often refractory to fluids
    • Lesions above T6: Consider norepinephrine or dopamine. ^[67]
    • Lesions below T6: Consider phenylephrine. ^[67]
  • Consider atropine or cardiac pacing to treat bradycardia; (see “Unstable bradycardia” for details). ^[70]
  • Consult a spine surgeon early to evaluate whether the patient is a candidate for urgent spinal decompression.
• Monitoring
  • Insert a urinary catheter early. ^[71]
  • Hemodynamic targets should be individualized in consultation with a specialist.
    • Avoid hypotension (systolic BP < 90 mm Hg).
    • Consider maintaining an MAP > 85–90 mm Hg during the first 5–7 days after injury. ^[67][68][69]
    • Laboratory perfusion parameters (e.g., lactate, base deficit) are typically more reliable markers of perfusion than MAP in patients with SCI.
  • Monitor for cardiovascular complications (e.g., ACS, stroke).
• Supportive care ^[67]
  • Prevent hypothermia ; monitor temperature frequently and use warm IV fluids or warming devices as needed.
  • Patients may have allodynia; careful patient handling and pain management are required.
  • Vasovagal responses can be increased and can lead to refractory shock.
  • Autonomic dysreflexia and vascular dysfunction may be present and can complicate management and recovery. ^[70][72]

Patients with neurogenic shock can have increased vasovagal responses to common procedures (e.g., suctioning, endotracheal intubation), which can trigger rapid changes in heart rate and blood pressure and increase the risk for complications and refractory shock. ^[73]

• General
  • Cardiovascular collapse
  • Acute renal failure (due to prolonged tissue hypoperfusion)
  • Delirium
• Specific shock subtypes
  • Airway obstruction (anaphylactic shock)
  • Pulmonary edema (cardiogenic shock)
  • Disseminated intravascular coagulation (hemorrhagic shock and septic shock)
• Iatrogenic
  • Nosocomial infections: e.g., CLABSI, VAP
  • Complications of mechanical ventilation
  • Complications of IV fluid therapy

Rescue therapies for shock are for patients who remain in shock despite adequate treatment of the underlying cause. These treatments should be given in consultation with a specialist, and they include: ^[3]

• Corticosteroids (e.g., hydrocortisone): for suspected critical illness-related corticosteroid insufficiency (CIRCI) ^[34][74]
  • Diagnosis of CIRCI is based on the presence of critical illness plus one of the following :
    • Increase in cortisol level of less than 9 mcg/dL after an ACTH stimulation test
    • Random plasma cortisol < 10–15 mcg/dL ^[34][74]
    • Positive hemodynamic response (e.g., reduced need for vasopressors) to hydrocortisone 50–300 mg IV
  • See also “Adrenal crisis.”
• Bicarbonate (e.g., 8.4% sodium bicarbonate ) ^[3]
  • For correction of severe metabolic acidosis (e.g., pH < 7.1)
  • Tailor treatment to the patient's bicarbonate deficit and monitor HCO₃ levels and pH frequently (e.g., initially every 2 hours). ^[75]
• Mechanical circulatory support
  • Consider ECMO for severe ARDS, refractory respiratory failure, or refractory heart failure.
  • Consider IABP and LVAD for refractory cardiogenic shock.

• One-Minute Telegram 8-2020-2/3: Should a cocktail of vitamin C, thiamine, and hydrocortisone be given to all patients with septic shock?

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